2. Disease Areas
  3. Cancer Digestive System Disease
  4. Colorectal Cancer Digestive System Cancer
  5. KRAS/Ras Mutation Colorectal Cancer

KRAS/Ras Mutation Colorectal Cancer

KRAS mutations are the most prevalent oncogenic alterations in colorectal cancer (CRC), occurring in approximately 45% of cases and driving tumor initiation and progression. These mutations are particularly common in microsatellite stable, right-sided CRC and are associated with a poorer prognosis. Importantly, KRAS mutations render tumors resistant to anti-EGFR therapies, making mutation testing essential for all patients with metastatic CRC. Although direct targeting of KRAS has historically been challenging, recent advances have led to the development of KRASG12C inhibitors, marking a significant breakthrough. This review outlines progress in direct KRAS inhibition, explores alternative therapeutic strategies for KRAS-mutant CRC, and summarizes key findings from completed and ongoing clinical trials.

KRAS/Ras Mutation Colorectal Cancer (7):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-12037
    Rigosertib sodium 592542-60-4 99.57%
    Rigosertib sodium (ON-01910 sodium) is a multi-kinase inhibitor and a selective anti-cancer agent, which induces apoptosis by inhibition the PI3K/Akt pathway, promotes the phosphorylation of histone H2AX and induces G2/M arrest in cell cycle. Rigosertib sodium is a selective and non-ATP-competitive inhibitor of PLK1 with an IC50 of 9 nM.
    Rigosertib sodium
  • HY-202699
    SHOC2-RAS PPI-IN-1 99.50%
    SHOC2-RAS PPI-IN-1 is a SHOC2-NRAS interaction inhibitor with IC50 of 0.048 μM and a Kd of 0.065 μM for SHOC2. SHOC2-RAS PPI-IN-1 inhibits RAS/MAPK signalling and downregulates MEK and ERK phosphorylation. SHOC2-RAS PPI-IN-1 can inhibit cells proliferation in RAS-mutant cancer models. SHOC2-RAS PPI-IN-1 can be used for the research of RAS-mutant cancers.
    SHOC2-RAS PPI-IN-1
  • HY-13495
    ML281 1404437-62-2 98.04%
    ML281 is a highly selective inhibitor of serine/threonine kinase 33 (STK33) with an IC50 value of 14 nM. ML281 shows 700-fold selectivity over PKA and 550-fold over AurB. ML281 exerts core mechanism by inhibiting STK33: in small cell lung cancer, ML281 downregulates RPS6/BAD signaling phosphorylation, induces apoptosis, and suppresses proliferation, invasion. ML281 reduces STK33-mediated 4-hydroxyphenylpyruvate dioxygenase (HPD) phosphorylation in tyrosinemia . ML281 is suitable for research on STK33 function, KRAS mutation-related cancers (pancreatic cancer, colon cancer, lung adenocarcinoma, etc.), small cell lung cancer, and tyrosinemia-related damage
    ML281
  • HY-P992409
    MEDI-5304
    MEDI-5304 is a hedgehog antibody inhibitor with human sonic hedgehog (SHH) KD of 5.13 pmol/L, and human Indian hedgehog (IHH) KD of 34.7 pmol/L. MEDI-5304 binds and neutralizes SHH and IHH, blocks downstream target gene transcription, inhibits osteoblast differentiation. MEDI-5304 can be used for the research of colon cancer.
    MEDI-5304
  • HY-183146
    CDK2-IN-57
    CDK2-IN-57 is a selective Cdk2/CycE inhibitor with an IC50 of 2.8 nM. CDK2-IN-57 inhibits Cdk1/2 kinase activity, blocks cell cycle progression, induces G0-phase cell cycle arrest, and prevents S-phase entry. CDK2-IN-57 can be used for the research of colon carcinoma.
    CDK2-IN-57
  • HY-124755
    RAS activator compound 1 1579978-17-8 98.90%
    RAS activator compound 1 (Compound 7c) is a RAS activator targeting the guanine nucleotide exchange factor (GEF) son of sevenless homologue 1 (SOS1). RAS activator compound 1 can activate the nucleotide exchange process and increase levels of active RAS-GTP in HeLa cells. RAS activator compound 1 can be used for research of RAS-driven tumor.
    RAS activator compound 1
  • HY-181284
    BYBC-1 2563902-57-6
    BYBC‑1 is a selective G4‑RNA‑targeting ligand with high affinity forKRAS and NRAS G4‑RNAs (Kd = 0.05-0.28 μM). BYBC‑1 stabilizes G4‑RNA structures in KRAS and NRAS mRNA, blocks thePI3K/AKT and MAPK/ERK pathways, activates the DNA damage response (DDR), suppresses energy metabolism, and induces S‑phase arrest and apoptosis. BYBC‑1 exhibits high selectivity over non‑malignant fibroblasts and significantly inhibits the growth of HCT‑116 xenograft tumors in vivo. BYBC‑1 can be used for the study of colorectal cancer.
    BYBC-1